Abstract
Background: Human immunodeficiency virus (HIV) infection with pronounced immunosuppression disrupts Epstein–Barr virus (EBV)–host balance with increased lymphoma risk. We explored whether different host responses to HIV are reflected in the EBV–host balance. Methods: Eleven unvaccinated HIV-positive patients and 16 participants in a vaccine trial were included in the study. Blood samples were collected, B cells extracted, and EBV DNA load was determined using a semiquantitative polymerase chain reaction (PCR) method. Results: Treatment-naïve patients with a history of symptomatic primary HIV infection showed non-significant, but higher EBV load compared to untreated long-term non-progressors. A significant difference in HIV RNA titres between these groups correlated weakly to EBV DNA load. Patients in the vaccine trial with recombinant HIV gp160 and/or adjuvant and with a history of symptomatic primary HIV infection, showed a 1-log increase in EBV load compared to patients with long-lasting HIV disease. Conclusion: Different host responses to HIV infection, especially in combination with vaccination, can be reflected in the EBV–host balance.
Acknowledgements
This study was supported by grants from the Swedish Cancer Society and the Research Council (VR). We are very grateful for the generous provision of patient samples by Britta Wahren and Eric Sandström, Karolinska Institute.
Declaration of interest: This study was supported by the Swedish Cancer Society and the Children's Cancer Foundation. No commercial relationship or potential conflict of interest related to the submission exists.